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1.2.1 Structure of a Bacteria and Antibiotic Resistance

Bacterial Structure and Antibiotics
by

Lori Richardson

on 18 September 2016

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Transcript of 1.2.1 Structure of a Bacteria and Antibiotic Resistance

Capsule
Cell Wall
Cell
Membrane
Serves as a barrier against phagocytosis
Maintains the shape of the bacteria
Transports nutrients and wastes
Nucleoid
Contains most of the bacterial DNA
Plasmid
Extra DNA that contains Antibiotic Resistance
Ribosomes
Carry out protein synthesis
Flagella
Movement of the cell
Pili
Movement of materials across the cell membrane
Endotoxins
Toxins known as LPS in a Gram Negative Bacteria that are released during lysis of the cell.
Gram Positive
Gram Negative
Penicillins
Sulfa Antibiotics
Fluoroquinolones
Tetracyclines
Penicillins work by interfering with the cell wall production. As the bacteria grows, the cell wall weakens and eventually ruptures.
Tetracyclines inhibit a lot of enzyme reactions essential for the vital processes of bacterial cells. The most sensitive biochemical reaction that is inhibited is the synthesis of proteins
Work on Gram Positive and Gram Negative
Works better on Gram Positive than Gram Negative
Fluoroquinolones work by preventing the supercoiling of DNA after replication. It also inhibits an enzyme used during replication and transcription.
Works on both Gram Positive and Gram Negative
Sulfa drugs work by binding and inhibiting a specific enzyme called dihydropteroate synthase (DHPS). This enzyme is critical for the synthesis of folate, an essential nutrient.
Works on both Gram Positive and Gram Negative
Penicillin, one of the first antibiotics to be used widely, prevents the final cross-linking step, or transpeptidation, in assembly of this macromolecule. The result is a very fragile cell wall that bursts, killing the bacterium. No harm comes to the human host because penicillin does not inhibit any biochemical process that goes on within us.
All cells require folic acid and it can diffuse easily into human cells. But the vitamin cannot enter bacterial cells and thus bacteria must make their own. The sulfa drugs such as sulfonamides inhibit a critical enzyme--dihydropteroate synthase--in this process. Once the process is stopped, the bacteria can no longer grow.
Tetracycline can cross the membranes of bacteria and accumulate in high concentrations in the cytoplasm. Tetracycline then binds to a single site on the ribosome--the 30S (smaller) ribosomal subunit--and blocks a key RNA interaction, which shuts off the lengthening protein chain. In human cells, however, tetracycline does not accumulate in sufficient concentrations to stop protein synthesis.
DNA replication must occur in both bacteria and human cells. The process is sufficiently different in each that antibiotics such as ciprofloxacin--a fluoroquinolone notable for its activity against the anthrax bacillus--can specifically target an enzyme called DNA gyrase in bacteria. This enzyme relaxes tightly wound chromosomal DNA, thereby allowing DNA replication to proceed. But this antibiotic does not affect the DNA gyrases of humans and thus, again, bacteria die while the host remains unharmed.
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